The major goal of this study was to determine whether myocardial contractile function durig the development of progressive coronary artery stenosis induced by ameroid constriction in conscious pigs reflected myocardial hibernation" or stunning". Minipigs were instrumented with a coronary ameroid constrictor and hydraulic occluder, regional wall thickness crystals, LV pressure gauge and aortic and left atrial catheters. In the 7 pigs in which it was mesured, systolic wall thickening distal to the ameroid fell by a maximum of 56q6% at 20q3days after ameroid implantation and then began to recover. At 1 day after ameroid implantation brief, complete coronary artery occlusion (CAO) resulted in wall thinning distal to the ameroid (-113q4%) and transmural decreases in myocardial blood flow in endo (from 0.82q0.08 to 0.02q0.01 ml/min/g) and epi (from 0.73q0.13 to 0.03q0.02 ml/min/g) layers. At 20q3 days baseline myocardial blood flow was not altered either in endo or epi layers, while brief complete CAO still reduced in WT (-83q12%) and myocardial blood flow in endo (to 0.21q0.03 ml/min/g) and epi (to 0.43 q 0.12 ml/min/g) layers, indicating that the coronary artery was not totally occluded. Pathology in 4 pigs demonstrated no gross necrotic myocarrdium shortly after this time point. Transient reductions in WT distal to the ameroid were observed during progressive coronary artery stenosis in response to spontaneous increases in activity. beat by beatanalysis of these episodes revealed that acute reductions in WT followed increases in LV dP/dt and heart rate, and exhibited delayed recovery. These data suggest that the reduced function during ameroid-induced coronary sstenosis reflected cumulative myocardial stunning rather than a primary deficit in coronary blood flow or hibernating myocardium".